In a normal heart, cells of the sinoatrial node (SA node) spontaneously depolarize and thereby initiate an action potential. This action potential propagates rapidly through the atria (which contract), slowly through the atrioventricular node (AV node), the atriventricular bundle (AV bundle or His bundle) and then to the ventricles, which causes ventricular contraction. Thus, in a normal heart, ventricular rhythm relies on conduction of action potentials through the AV node and AV bundle.
Disruption of action potentials in an atrium and/or a ventricle can lead to arrhythmias. Arrhythmias are generally classified as supraventricular arrhythmias and ventricular arrhythmias. Supraventricular arrhythmias (SVAs) are characterized by abnormal rhythms that may arise in the atria or the atrioventricular node (AV node). For example, a paroxysmal SVA can exhibit heart rates between approximately 140 beats per minute (bpm) and approximately 250 bpm. However, the most common SVAs are typically atrial flutter and atrial fibrillation. In addition, many SVAs involve the AV node, for example, AV nodal reentry tachycardia (AVNRT) where an electrical loop or circuit includes the AV node.
Atrial flutter can result when an early beat triggers a “circus circular current” that travels in regular cycles around the atrium, pushing the atrial rate up to approximately 250 bpm to approximately 350 bpm. The atrioventricular node between the atria and ventricles will often block one of every two beats, keeping the ventricular rate at about 125 bpm to about 175 bpm. This is the pulse rate that will be felt, even though the atria are beating more rapidly. At this pace, the ventricles will usually continue to pump blood relatively effectively for many hours or even days. A patient with underlying heart disease, however, may experience chest pain, faintness, or even heart failure as a result of the continuing increased stress on the heart muscle. In some individuals, the ventricular rate may also be slower if there is increased block of impulses in the AV node, or faster if there is little or no block.
If the cardiac impulse fails to follow a regular circuit and divides along multiple pathways, a chaos of uncoordinated beats results, producing atrial fibrillation. Fibrillation commonly occurs when the atrium is enlarged (usually because of heart disease). In addition, it can occur in the absence of any apparent heart disease. In fibrillation, the atrial rate can increase to more than 350 bpm and cause the atria to fail to pump blood effectively. Under such circumstances, the ventricular beat may also become haphazard, producing a rapid irregular pulse. Although atrial fibrillation may cause the heart to lose approximately 20 to 30 percent of its pumping effectiveness, the volume of blood pumped by the ventricles usually remains within the margin of safety, again because the atrioventricular node blocks out many of the chaotic beats. Hence, during atrial fibrillation, the ventricle may contract at a lesser rate than the atria, for example, of approximately 125 bpm to approximately 175 bpm.
Overall, SVAs are not typically immediately life threatening when compared to ventricular arrhythmias. Ventricular arrhythmias include ventricular tachycardia and ventricular fibrillation, which typically originate in the ventricles. Ventricular arrhythmias are often associated with rapid and/or chaotic ventricular rhythms. For example, sustained ventricular tachycardia can lead to ventricular fibrillation. In sustained ventricular tachycardia, consecutive impulses arise from the ventricles at a rate of 100 bpm or more. Such activity may degenerate further into disorganized electrical activity known as ventricular fibrillation. In ventricular fibrillation, disorganized action potentials can cause the myocardium to quiver rather than contract. Such chaotic quivering can greatly reduce the heart's pumping ability. Indeed, approximately two-thirds of all deaths from arrhythmia are caused by ventricular fibrillation. A variety of conditions such as, but not limited to, hypoxia, ischemia, pharmacologic therapy (e.g., sympathomimetics), and asynchronous pacing may promote onset of ventricular arrhythmia.
As described above, SVAs and ventricular arrhythmias may lead to ventricular rates in excess of 100 bpm; hence, discrimination of ventricular arrhythmias from SVAs may require more than just knowledge of ventricular rate. In addition, most implantable stimulation devices do not have an ability to adequately discriminate between SVA and ventricular arrhythmias. Further, implantable devices having antitachycardia pacing, cardioversion stimulus and/or defibrillation shock capabilities may use such capabilities inappropriately to treat elevated ventricular rates originating from SVAs. Therefore, a need exists for methods and/or devices to discriminate between arrhythmias. Various exemplary methods and/or devices are described below which optionally address this need and/or other needs.